The green-peach aphid Myzus persicae (Hemiptera: Aphididae) is a pest of crop plants worldwide. Aphids are phloem-feeding insects, and they inflict damage through direct effects of feeding, and indirectly by transmission of plant viruses. Development of insecticide resistance in aphids has motivated the development of novel control strategies. New approaches to pest control may be informed by an enhanced understanding of the genes allowing aphids to subsist on the nutritionally unbalanced diet of phloem sap, and to detoxify chemical defenses presented by a wide range of hosts. Certain lineages of M. persicae have expanded their host range to include tobacco in agricultural settings, and an objective of this research is to characterize differences between adapted and non-adapted lineages in their ability to accept tobacco as a suitable host in the laboratory, and to tolerate tobacco-specific defenses. Tobacco-adapted aphids are highly resistant to nicotine, a potent neurotoxic plant defense, and may be stimulated to feed on nicotine-containing diets by associating nicotine as a characteristic of a suitable host plant. A platform for functional genomics studies of M. persicae has been established by sequencing expressed genes from a diversity of aphid tissues. Bioinformatic analysis of these sequences allowed for the development of an annotated microarray containing fragments of over 10,000 aphid genes, which has been used to study gene expression changes in the heads of tobacco-adapted aphids in response to nicotine. Several induced genes are associated with aphid salivation and detoxification of plant defenses. The availability of the whole genome sequence for the closely related pea aphid, Acyrthosiphon pisum, has facilitated the annotation of M. persicae genes, and allowed for comparison of gene content in the two species. Annotation of pea aphid genes involved in nucleotide metabolism revealed an unexpected loss of purine catabolic capability in the pea aphid. Data from genome analysis of A. pisum and its bacterial endosymbiont Buchnera aphidicola suggests a shared purine metabolic pathway, which may have led to the loss of key aphid purine salvage genes.